作者: GANTA VIJAY CHAITANYA , WALTER CROMER , SHANNON WELLS , MERILYN JENNINGS , JAMES M MATHIS
DOI: 10.1111/J.1549-8719.2011.00141.X
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摘要: Please cite this paper as: Chaitanya GV, Cromer W, Wells S, Jennings M, Mathis JM, Minagar A and Alexander JS. Metabolic Modulation of Cytokine-Induced Brain Endothelial Adhesion Molecule Expression. Microcirculation 19: 155–165, 2012. Abstract Objective: Cytokines contribute to cerebro-vascular inflammatory immune responses by inducing ECAMs’ expression. Ischemic insults can be separated into aglycemic hypoxic components. However, whether aglycemia, hypoxia or OGD plays a major role in dysregulating BBB promotes cell infiltration via expression is not clear. We investigated how ICAM-1, VCAM-1, MAdCAM-1, PECAM-1, E- P-selectin response TNF-α, IL-1β IFN-γ was altered aglycemia (A), (H) combined oxygen glucose deprivation (OGD). Methods: surface enzyme linked immunoabsorbent assay (cell ELISA) used analyze ECAM expression. Results: observed that ICAM-1 PECAM-1 expressions were insensitive hypoxia, OGD. Conversely, VCAM-1 E-selectin increased but aglycemia. MAdCAM-1 induced decreased Patterns cytokine-regulated also modified metabolic conditions. Conclusions: Our results indicate patterns inflammation-associated ECAMs represent cumulative influences from stressors, as well cytokine activation. The following tissue injury reflects mechanistic interactions between disturbances, alterations cytokines. Normalization metabolism, profiles, may provide important targets for therapeutic treatment inflammation.